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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Acta Naturae</journal-id><journal-title-group><journal-title xml:lang="en">Acta Naturae</journal-title><trans-title-group xml:lang="ru"><trans-title>Acta Naturae</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2075-8251</issn><publisher><publisher-name xml:lang="en">Acta Naturae Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">10351</article-id><article-id pub-id-type="doi">10.32607/20758251-2018-10-1-15-23</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Reviews</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Обзоры</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">The Role of TAL1 in Hematopoiesis and Leukemogenesis</article-title><trans-title-group xml:lang="ru"><trans-title>TAL1: его роль в гемопоэзе и в злокачественном перерождении клеток крови</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Vagapova</surname><given-names>E. R.</given-names></name><name xml:lang="ru"><surname>Вагапова</surname><given-names>Э. Р.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>elmira-mi@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Spirin</surname><given-names>P. V.</given-names></name><name xml:lang="ru"><surname>Спирин</surname><given-names>П. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>elmira-mi@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Lebedev</surname><given-names>T. D.</given-names></name><name xml:lang="ru"><surname>Лебедев</surname><given-names>Т. Д.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>elmira-mi@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Prassolov</surname><given-names>V. S.</given-names></name><name xml:lang="ru"><surname>Прасолов</surname><given-names>В. С.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>elmira-mi@mail.ru</email><xref ref-type="aff" rid="aff2"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">The Engelhardt Institute of Molecular Biology, Russian Academy of Sciences</institution></aff><aff><institution xml:lang="ru">Институт молекулярной биологии им. В. А. Энгельгардта РАН</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">The Engelhardt Institute of Molecular Biology, Russian Academy of Sciences</institution></aff><aff><institution xml:lang="ru">Институт молекулярной биологии им. В. А. Энгельгардта РАНИнститут молекулярной биологии им. В. А. Энгельгардта РАН</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2018-03-15" publication-format="electronic"><day>15</day><month>03</month><year>2018</year></pub-date><volume>10</volume><issue>1</issue><issue-title xml:lang="en">VOL 10, NO1 (2018)</issue-title><issue-title xml:lang="ru">ТОМ 10, №1 (2018)</issue-title><fpage>15</fpage><lpage>23</lpage><history><date date-type="received" iso-8601-date="2020-01-17"><day>17</day><month>01</month><year>2020</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2018, Vagapova E.R., Spirin P.V., Lebedev T.D., Prassolov V.S.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2018, Вагапова Э.Р., Спирин П.В., Лебедев Т.Д., Прасолов В.С.</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="en">Vagapova E.R., Spirin P.V., Lebedev T.D., Prassolov V.S.</copyright-holder><copyright-holder xml:lang="ru">Вагапова Э.Р., Спирин П.В., Лебедев Т.Д., Прасолов В.С.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://actanaturae.ru/2075-8251/article/view/10351">https://actanaturae.ru/2075-8251/article/view/10351</self-uri><abstract xml:lang="en"><p>TAL1 (SCL/TAL1, T-cell acute leukemia protein 1) is a transcription factor that is involved in the process of hematopoiesis and leukemogenesis. It participates in blood cell formation, forms mesoderm in early embryogenesis, and regulates hematopoiesis in adult organisms. TAL1 is essential in maintaining the multipotency of hematopoietic stem cells (HSC) and keeping them in quiescence (stage G0). TAL1 forms complexes with various transcription factors, regulating hematopoiesis (E2A/HEB, GATA1-3, LMO1-2, Ldb1, ETO2, RUNX1, ERG, FLI1). In these complexes, TAL1 regulates normal myeloid differentiation, controls the proliferation of erythroid progenitors, and determines the choice of the direction of HSC differentiation. The transcription factors TAL1, E2A, GATA1 (or GATA2), LMO2, and Ldb1 are the major components of the SCL complex. In addition to normal hematopoiesis, this complex may also be involved in the process of blood cell malignant transformation. Upregulation of C-KIT expression is one of the main roles played by the SCL complex. Today, TAL1 and its partners are considered promising therapeutic targets in the treatment of T-cell acute lymphoblastic leukemia.</p></abstract><trans-abstract xml:lang="ru"><p>TAL1 (SCL/TAL1, T-cell acute leukemia protein 1) - транскрипционный фактор и один из основных участников гемопоэза. TAL1 участвует в процессах дифференцировки клеток крови из мезодермы на ранних стадиях эмбриогенеза и регулирует гемопоэз в зрелом организме. TAL1 необходим для сохранения мультипотентности гемопоэтических стволовых клеток (ГСК) и удержания их в фазе покоя G0. TAL1 формирует комплексы с различными транскрипционными факторами-участниками гемопоэза (E2A/HEB, GATA1-3, LMO1-2, Ldb1, ETO2, RUNX1, ERG, FLI1). В составе таких комплексов TAL1 участвует в нормальной дифференцировке кроветворных клеток миелоидного ряда, контролирует пролиферацию эритроидных предшественников, а также определяет выбор направления дифференцировки ГСК. SCL-комплекс, основными компонентами которого являются TAL1, E2A, GATA1 (или GATA2), LMO2 и Ldb1, может участвовать в злокачественном перерождении клеток крови. Одна из ключевых ролей SCL-комплекса в канцерогенезе - позитивная регуляция экспрессии рецепторной тирозинкиназы C-KIT. В настоящее время TAL1 и его партнеры рассматриваются в качестве перспективной терапевтической мишени при острых лимфобластных лейкозах.</p></trans-abstract><kwd-group xml:lang="en"><kwd>hematopoiesis</kwd><kwd>acute myeloid leukemia</kwd><kwd>receptor tyrosine kinase C-KIT</kwd><kwd>T-cell acute lymphoblastic leukemia</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>гемопоэз</kwd><kwd>острый миелоидный лейкоз</kwd><kwd>рецепторная тирозинкиназа C-KIT</kwd><kwd>T-клеточный острый лимфобластный лейкоз</kwd></kwd-group><funding-group><funding-statement xml:lang="en">This study was carried out as a part of the Program for Basic Research of the State Academies of Sciences in 2013–2020 (topic No 01201363823) and supported by the Russian Science Foundation (Project No 14-50-00060).</funding-statement><funding-statement xml:lang="ru">Работа выполнена в рамках Программы фундаментальных исследований государственных академий наук на 2013–2020 годы (тема № 01201363823) за счет средств Российского научного фонда (проект № 14-50-00060).</funding-statement></funding-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>[1] Hoang T., Lambert J.A., Martin R. // Curr. 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